Vibrio, Campylobacter, Helicobacter Flashcards
Where vibrios are found ?
Mainly in water
Widespread in nature
Vibrios characteristics?
Short, curved, gram negative bacilli ( color pink or red)
Motile
Oxidase positive
Mention non halophilc vibrios ( cant live in salt water) ?
V.cholerae
Mention halophilic vibrios
V.parahemolyticus
V.vulnificus
How do vicholerae transmit ?
By drinking contaminated water
There is no need for vector
What is the habitat for vicholerae ?
Water contaminated with fece s of patients or carriers
Epidemiology of vicholerae 8
Pandemis and epidemics : cindia and bangladish, east asia, africa)
Morphology of vicholerae?
Gram-negative slender bacilli (comma shaped) motile , non-capsulated
Culture of v.cholerae?
Aerobe
Enrichment media : alkaline peptone water.
Selective media : tcbs media
Observe yellow colonies
Laboratory diagnosis of v.cholerae
Somatic (o) antigen structure
V.cholerae: ol antigen (vibrio cholerae o1)
Non o1 v.cholerae: no antigen
What is the pathogenisity of v.cholerae ?
- febrile diarhoeal illness (sever)
- vomiting
- rapid dehydration and hypovolemic shock
- death can occur in 12-24 hrs
- Produce enteritoxin
- Causes irreversible activation of cAMP
- Blocks the uptake of water which accompanies Na and Cl absorption
- Passive movement of water leading to serious loss of water
- Infective dose is small
- Multiply in small intestine
V.cholerae non 01 pathogenisity (without somatic antigen) :
- causes mild, sometimes bloody diarrhoea
- accompanied by abdominal cramps
- may produce toxins
- can also cause epidemics
V.parahemolyticus
Halophilic or non halophilic vibrio?
Halophilic vibrio (salt-tolernt)
What does v. Parahemolyticus Cause?
Acute gastroenteritis (food poisoning)
Pathogenisity of parahemolyticus:
causes explosive diarrhoea
Self limiting (3 days)
Abdominal pain, nausea and vomiting
Related to ingestion of sea food (fish and shellfish)→ not only man there is a vector that transmit the disease.
Laboratory diagnosis of v.parahemolyticus :
Non-sucrose fermenter on tcbs
Green colonies
V.vulnificus : halophilc or non halophilic vibrio
What it is associated with ?
Halophilic vibrio
it is associated with warm water environment
What are the 3 main clinical syndromes of v.vulnificus?
- Rapid onset fulminating septicemia followed by cutaneous lesions shell fish )
- Rapid onset cellulitis
- Acute diarrhoea following consumption of shell fish .
What is the pathogenesis of v.vulnificus?
Virulence associated with polysacchride capsule.
What are the characteristics of campylobacter ?
1.c.jejuni 2.c.coli Small spiral gram negative bacilli Motile No spores Oxidase positive
C. Jejuni and c-coli pathogenesis
caused by food poisoning
Infection acquired by ingestion
The commonest cause of infective diarrhea in developed conntries. Animals are the main source : poultry and raw meat.
Small infective dose
Involvement of both small and large intestine
Causes invasive disease
Do not multiply in food (salmonellosis)
C. Jejuni andc.coli clinical manifestation.
Sever abdominal pain diarrhoeal /bloody Fever Complications: gi hemorrhage toxic megacolon hus reactive arthritis
C. Jejuni and c.coli laboratory diagnosis
Stool Culture Selective media: charcoal -based media containing antibiotics microaerophilic environment for growth Temperature 42 -43°c c.jejuni (the commenest) : Hydrolyse hippurate 90-95% of infections
Helicobacter pylori description:
Gram -negative spirally-shaped
microcerophilic
man appears to be the only reservoir
oral-oral or facal-oral rout for transmission
Helicobacter pylori pathogenesis:
Live only in gastric mucosa
ip few days
symptoms of abdominal pain , nausea
lasts for 2 weeks
minority of patients develop peptic ulcer
long standing infection associated gastric cancer
Helicobacter pylori labratory diagnosis:
Invasive tests :
sample of gastric mucosa
microscopy
culture
biopsy urease test (small portion of the biopsy put in small quantity of urease solution (indicator, amonia production and change in ph)
Non invasive tests :
Serology :ELISA
Urea breath
Peptic ulceration : pathogenic mechanism
The production of amonia by urease which causes ionic changes in the mucus layer of the stomach
Production of toxins as lipopolysaccharide that activate inflammatory cells
Stimulation of an auto-immune response by production of antigens that cross-react with antral gastric antigens
The degradation of mucus by a protease
